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We present the first case report of a successful laparoscopic complete excision of a splenic lymphangioma. The splenic tumor was preoperatively diagnosed to be a lymphangioma by the combined modalities of ultrasonography, computed tomography, magnetic resonance imaging, and angiography. A laparoscopic splenectomy was subsequently performed and the pathological examination of the mass confirmed the diagnosis of a lymphangioma. Based on the above findings, a laparoscopic splenectomy is recommended when a splenic tumor is suspected to be either benign or borderline.

Plasma fibronectin (FN) has a broad range of biological functions involved in cellular adhesion, motility, differentiation, apoptosis, hemostasis, wound healing, reticuloendothelial system function, and ischemic injury. In this study, we examined the effects of FN on D-galactosamine (GalN)/lipopolysaccharide (LPS)-induced fulminant liver failure in mice. Female Balb/c mice received intraperitoneal injection of 50 mg/kg of LPS and 400 mg/kg of GalN simultaneously. Thirty minutes before GalN/LPS administration, human plasma FN (FN group) or the same dose of human serum albumin (control group) was given intravenously. GalN/LPS induced a marked decrease in plasma FN, which was reversed by FN pretreatment. The survival rate of the FN group was markedly improved in a dose-dependent manner compared with that of the control group (survival rate 0%). FN prevented increases in the concentrations of serum enzymes and total bilirubin related to liver injury. FN pretreatment significantly suppressed tumor necrosis factor (TNF)-a, interferon (IFN)-g, and interleukin (IL)-6 levels, and enhanced IL-10 levels in serum and liver tissue compared with the control group. Moreover, TUNEL staining, caspase 3 and 8 activities, and necrosis in the remnant liver were significantly decreased in the FN-treated rats compared with the controls. Furthermore, FN pretreatment inhibited the activation of nuclear factor (NF)-kB and increased the expression of Bcl-xL protein in liver tissue. These results suggest that FN protected against GalN/LPSinduced liver failure by a mechanism involving inhibition of NF-kB activation, which caused down-regulation of TNF-a and involved up-regulation of IL-10, and elevation of Bcl-xL induced a blockage of apoptotic signals, by which apoptosis of hepatocytes caused by GalN/LPS was suppressed.

We report a rare case of amyloidosis of the gallbladder in a 63-year-old woman with a history of primary amyloidosis. The patient was asymptomatic. Blood chemistry and hematologic laboratory levels, as well as values for tumor markers, were unremarkable. Ultrasonography (US) of the abdomen showed a focal echogenic lesion (22 x 15 mm) in the body of the gallbladder, and moderate enhancement was noted on contrast-enhanced US. Abdominal computed tomography revealed nodular wall thickening in the body of the gallbladder that was enhanced by contrast material. Although this patient was asymptomatic, the existence of gallbladder cancer could not be totally denied. Therefore, laparoscopic cholecystectomy was performed for total biopsy of the gallbladder. An intraoperative frozen-section examination revealed evidence of mild chronic cholecystitis with the appearance of hyalinal stroma. There was no malignant lesion. The final diagnosis, amyloidosis of the gallbladder, was obtained by alkaline alcoholic Congo red staining. Amyloid depositions were found in the walls of the vessels in the submucosa and the lamina propria mucosae, consistent with an elevated nodular lesion in the body of the gallbladder. To our knowledge, this is the first case of amyloidosis of the gallbladder mimicking gallbladder cancer that was diagnosed after laparoscopic cholecystectomy.